Acute kidney injury (AKI), also called acute renal failure (ARF), is a rapid loss of kidney function. The causes of AKI are numerous and may include low blood volume, decreased blood flow to the kidneys, exposure of the kidney to toxic substances, or urinary tract obstruction. AKI is diagnosed on the basis of clinical history and laboratory data. Kidney function may be measured by serum creatinine or urine output, among other tests, and a rapid reduction in either or both of these factors may be diagnosed as AKI.
One possible cause of AKI is the use of intravascular iodinated contrast media or contrast agents. Contrast-induced AKI (CI-AKI) is a common problem in patients receiving intravascular iodine-containing contrast media for angiography. CI-AKI is associated with excessive hospitalization cost, morbidity, and mortality. Clinical procedures involving intravascular iodine-containing contrast media injection may include, for example, percutaneous coronary intervention (PCI), peripheral vascular angiography and intervention, transarterial heart valve interventions, and neurological angiography and intervention. In clinical practice, CI-AKI is diagnosed when serum creatinine levels increase by more than either 25% or 0.5 mg/dL above baseline within 48 to 72 hours of exposure to contrast media in the absence of other culprit etiology for AKI.
Management of AKI hinges on identification and treatment of the underlying cause. Additionally, management of AKI routinely includes avoidance of substances toxic to the kidneys, called nephrotoxins. Nephrotoxins include, for example, non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, iodinated contrast agents, such as those used for CT scans, many antibiotics, such as gentamicin, and a range of other substances.
Renal function monitoring by serum creatinine and urine output is routinely performed. For example, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate. In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improve renal function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid. Should low blood pressure prove a persistent problem in the fluid-replete patient, inotropes such as norepinephrine and dobutamine may be given to improve cardiac output and enhance renal perfusion. Also, while a useful pressor, there is no evidence to suggest that dopamine is of any specific benefit, and may in fact be harmful.
The myriad causes of intrinsic AKI can require specific therapies. For example, intrinsic AKI due to Wegener's granulomatosis may respond to steroid medication while toxin-induced prerenal AKI often responds to discontinuation of the offending agent, which may for example be aminoglycoside, penicillin, NSAIDs, or paracetamol. Obstruction of the urinary tract may also cause AKI and treatment may require relief of the obstruction, for example with a nephrostomy or urinary catheter.
Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI. A systematic review of the literature in 2008 shows no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration (CVVH). Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis.
Current prevention strategies for AKI, particularly for CI-AKI, are mainly supportive. They include for example (1) evaluating and stratifying patients with Mehran risk score before performing PCI, (2) avoiding high-osmolar contrast media by using low-osmolar or iso-osmolar contrast media, (3) reducing the amount of contrast media during PCI, (4) applying intravenously isotonic sodium chloride solution or sodium bicarbonate solution hours before and after PCI, and (5) avoiding use of nephrotoxic drugs (such as nonsteroidal anti-inflammatory drugs, aminoglycosides antibiotics, etc.). (See Stevens 1999, Schweiger 2007, Solomon 2010.) However, none of these strategies have proven to be consistently effective in preventing CI-AKI.